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Y1 LCRS Endocrinology > 9 The Adrenals and their Hormones > Flashcards

9 The Adrenals and their Hormones Flashcards

1
Q

Q: Where are the adrenal glands? Aka?

A

A: Embedded on the superior pole of each of the two kidneys

Sometimes called the suprarenal glands

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2
Q

Q: How many arteries and veins do the adrenal glands have? What does each one drain into?

A

A: many arteries but one vein (heavily perfused tissue)

left adrenal vein drains into renal vein

right adrenal veins drains into IVC-> heart

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3
Q

Q: Label a cross section of an adrenal gland. (6)

A

A: oval with a centre and 3 rings

tributary of central vein in medulla

centre= adrenal medulla

outer part of the adrenal gland is the Cortex which has 3 zones:

  • Zona Glomerulosa
  • Zona Fasciculata
  • Zona Reticularis

capsule on outside

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4
Q

Q: How does the structure vary in the adrenal cortex? (2) Describe blood flow. (3)

A

A: Zona Fasciculata - the cells line up as strings

Zona Reticularis doesn’t really have a pattern

blood flow to the adrenal cortex is from the arteries that feed the outside of the gland

blood then heads towards tributary of central vein via 2 methods:

  1. most passes through cells
  2. some vessels which go through the cortex to get to the adrenal medulla
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5
Q

Q: How does hormone production vary in the adrenal glands? (2)

How does one affect the other?

A

A: medulla produces catecholamine hormones

cortex produces corticosteroid hormones

as corticosteroids move towards central vein, there is a positive effect on promoting noro and adrenaline production

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6
Q

Q: Give 3 examples of hormones produced by the medulla. Type?

A

A: catecholamine hormones:

  • adrenaline 60% (epinephrine)
  • noradrenaline 20% (norepinephrine)
  • dopamine in small amounts
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7
Q

Q: Give 3 examples of hormones produced by the cortex. Type?

A

A: corticosteroid hormones:

  • mineralocorticoids (aldosterone)
  • glucocorticoids (cortisol)
  • sex hormones (androgens, oestrogens)
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8
Q

Q: How do cortical cells produce hormones? (5) How do you get specific hormones?

A

A: corticoSTEROID hormones

  1. cholesterol is delivered and stored as FA esters in cell cytoplasm
  2. stimulus causes esterase to liberate cholesterol
  3. StAR protein takes cholesterol into mitochondria
  4. hormone is produced
  5. released from mito and not stored because they are lipophilic and can pass easily through the membranes

depends on the enzymes present

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9
Q

Q: What’s the precursor of aldosterone? What’s the precursor of oestrogens?

A

A: progesterone

androgens

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10
Q

Q: What can cholesterol become in the adrenals? (3) gonads? (3)

A

A: - Mineralocorticoids (C21)

  • Glucocorticoids (C21)
  • (Androgens)
  • Progestogens (C21)
  • Androgens (C19)
  • Oestrogens (C18)
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11
Q

Q: Which enzyme is present to produce aldosterone but not present for cholesterol? (2)

A

A: aldosterone synthase

lacking P450c17

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12
Q

Q: Which enzyme is present to produce sex steroids but not present for cholesterol? (4)

A

A: 17,20 lyase

17 beta HSD

aromatase

P450c5

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13
Q

Q: What happens once corticosteroids are made? Transport? (2)

A

A: move straight into blood stream- are very lipid soluble and pass through bilayer

  • if unbound will be taken up cells
  • when bound protein= protected
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14
Q

Q: Compare aldosterone and cortisol transport. (3)

A

A: aldosterone:

  • 40% unbound= BIOACTIVE
  • 15% CBG bound
  • 45% albumin bound

cortisol:

  • 10% unbound= BIOACTIVE
  • 80% CBG bound
  • 10% albumin bound

cortisol is more selective for corticosteroid binding protein

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15
Q

Q: Why does the concentration of cortisol and aldosterone vary? Figures? Difference?

A

A: cortisol= diurnal- changes in day (higher in morningwhile you sleep/)
-cortisol is released in PULSES - so there will be pulsatile release on top of the circadian rhythm

8am= 140-690nmol/l
4pm= 80-330nmol/l

aldosterone- NOT controlled by the pituitary so the time of day is NOT important - but your position is important because aldosterone is involved in the control of fluid and balance

140-560pmol/l

1000fold difference (more cortisol)

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16
Q

Q: Which receptor does cortisol bind to? Aldosterone? Explain the situation.

A

A: -both bind to aldosterone receptors (MR= mineralocorticoids)
-cortisol also binds to glucocorticoid receptors (GR)

The concentration of cortisol in the blood is about 1000 times greater than that of aldosterone but cortisol isn’t constantly binding with MR because:

  • The kidneys have an enzyme which converts bioactive CORTISOL to CORTISONE (inactive)
  • Enzyme: 11b-hydroxysteroid dehydrogenase 2
  • This enzyme constantly removes the cortisol so it doesn’t interfere with the mineralocorticoid receptors
17
Q

Q: Where is aldosterone specifically made?

A

A: Zona Glomerulosa

18
Q

Q: Explain the process of aldesterone production. (4)

A

A: 1. LIVER produces ANGIOTENSINOGEN (a large protein)

  1. Renin (released by juxta-glomerular cells= in kidneys) breaks down angiotensinogen to ANGIOTENSIN I
  2. Then, ACE (angiotensin converting enzyme= abundant in lungs) converts angiotensin I to ANGIOTENSIN II
  3. ANGIOTENSIN II stimulates the zona glomerulosa to produce aldosterone by binding to receptors
19
Q

Q: What does ANGIOTENSIN II do? (2)

A

A: - the zona glomerulosa to produce aldosterone

-VASOCONSTRICTOR

20
Q

Q: What affects aldosterone production? (4)

A

A: -renin

  • Corticotrophin has a permissive effect - it will enhance the renin-angiotensin system
  • If the blood plasma sodium ion concentration falls, it has a direct effect in stimulating aldosterone production - so there is more sodium reabsorption and sodium concentration returns to normal
  • increase in potassium concentration stimulates aldosterone production leading to increased secretion of potassium
21
Q

Q: What causes the secretion of renin? where? What is the effect of this?

A

A: low renal perfusion pressure RPP in afferent arteriole leading to glomerulus

granular cells

causes production of substances -> that lead to production of substances -> lead to constriction of efferent arteriole

=> pressure builds back up and RPP increases

22
Q

Q: Aside from RPP, what causes the secretion of renin? (2)

A

A: renal sympathetic activity- fight/flight response increases renin production

decreased Na+ load passing through distil convoluted tubule

  • Na+ moves out from surrounding cells and enters lumen
  • cells shrink and cause renin production
  • aldosterone will promote Na reuptake
23
Q

Q: Describe the hypothalamo-pituitary-adrenocortical axis. (6) Graph?

A

A: stressor ->

hypothalamic hormones = CRH ->

pitutiary gland -> acts on corticotrophs (basophilic cells in the anterior pituitary)

  • > ACTH production
  • > affect adrenal gland
  • > cortisol production

both ACTH and cortisol show diurnal rhythm (low between 8am and 8pm and small spikes as cortisol is released in pulses)

24
Q

Q: Name a large stimulus for cortisol secretion. Examples? (3) Baseline?

A

A: stress

bacterial infection
physical trauma
exam stress

constantly produced, stressed or not

25
Q

Q: Where does aldosterone act? (2) Important to? (4) Summarise what it stimulates. (3)

A

A: distal convoluted tubule and cortical collecting duct

liver
sweat glands
gastric glands
colon

Stimulates

  • Na+ reabsorption
  • K+ secretion
  • H+ secretion -> have an effect on pH regulation of the blood
26
Q

Q: What is the mechanism of aldosterone action? (8)

A

A: 1. Being a steroid hormone, aldosterone passes through cell membranes

  1. binds to intracellular receptors (MR)
  2. hormone-receptor complex moves to the nucleus and attaches to the DNA
  3. switches on particular genes - it acts as a transcription factor
  4. Many of the proteins produced will be enzymes or pumps
  5. Aldosterone stimulates the synthesis of ion channels - in particular, sodium ion channels in the apical membrane (BRING Na INTO CELL)
  6. proteins produced may stimulate pumps like ATPase pump on the basolateral membrane which pumps sodium into the blood (Na FROM CELL TO INTERSTITIUM CONTAINING BLOOD)
  7. aldosterone doesn’t directly affect water but because Na flow is affected-> indirect effect: taken from lumen and to blood via AQP3/4 on basolateral side
27
Q

Q: What is the result of aldosterone action? (2)

A

A: proteins produced may stimulate pumps like ATPase pump on the basolateral membrane which pumps sodium into the blood

Aldosterone stimulates the synthesis of ion channels - in particular, sodium ion channels in the apical membrane

28
Q

Q: What is the mechanism of cortisol action?

A

A: 1. steroid hormone so enters cell

  1. binds to GR/MR (MR in most cells)
  2. hormone-receptor complex moves to the nucleus and attaches to the DNA
  3. has genomic effect
  4. causes production of mRNA/ new protein
29
Q

Q: Draw a graph of circulating levels of glucocorticoids (X) and cognitive performance (Y). What is needed for optimal activity? What happens when you’re stressed? Effect?

A

Q: REFER

low ratio: v little MR

opt= high ratio: just a little less GR= maximal MR stimulation (not in tissues with enzyme protection)

stress= low ratio= maximal GR

  • > fine if acue
  • > prolonged= problem
30
Q

Q: What are the metabolic of cortisol? (4)

A

A: 1. allows blood glucose to increase (predominantly effect in liver)

  1. get less transporters that take glucose into cells/tissues eg skeletal muscle
  2. tends to promote glycolysis
  3. physiological level-> stimulate gluconeogenesis
31
Q

Q: How does cortisol affect memory? (3) Stress? (2)

A

A: important for memory formation

cortisol increases hippocampus sensitivity to serotonin (upregulates serotonin 5HT 1A receptors)

serotonin intervention promotes granule cell division= cells that allow extra connection within memory formation

  • acute stress response= powerful effect on memory
  • problem if chronic
32
Q

Q: How does the type of receptor affect the effect of cortisol on memory? (2)

A

A: physiologically- MR is the major receptor = cortisol is pro memory

chronically- GR is major = cortisol and serotonin work against eachother -> becomes antimemory (REFER TO GRAPH OF RECEPTOR USE)

33
Q

Q: What are the immunological effects of cortisol? (5)

A

A: anti-inflammatory

  • decrease leukocyte function
  • decrease histamine production

immunosuppressive

  • decreased lymphocyte and monocyte function
  • decrease compliment levels

anti allergic action

34
Q

Q: How does caffeine affect cholesterol? alcohol? Prolonged?

A

A: both increase

alcohol= powerful

levels become suboptimal

35
Q

Q: What effect would supraphysiological levels of cortisol have on blood pressure? (4) Called? Where?

A

A: cortisol will get through that enzyme barrier

  • > eventually huge Na reuptake
  • > increase water retention
  • > increase bp (cortisol acts as aldosterone when in high amounts) CALLED CORTISOL INDUCED HYPERTENSION

DISTAL TUBULE CELL

36
Q

Q: Where are adrenal androgens produced? as? (3)

A

A: zona reticularis

  • DHEA: dehydroepiandrostenedione
  • DHEAS
  • androstenedione
37
Q

Q: What is the effect of adrenal androgens? therefore?

A

A: weak biological effect generally

converted into more active androgens eg testosterone by enzymes in peripheral tissues

38
Q

Q: How does the effect of adrenal androgens vary in men and women?

A

A: women: adrenal production of DHEA and DHEA-S contributes substantially to overall androgen production and effects

men: the adrenal contribution to androgen production is very small

increased effect in women than men

Y1 LCRS Endocrinology (19 decks)

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